ArticleOncogene2013
Ionizing radiation induces a dramatic persistence of p53 protein accumulation and DNA damage signaling in mutant p53 zebrafish.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- Review
- Integrated analysis of transcriptomic and metabolomic profiling reveal the p53 associated pathways underlying the response to ionizing radiation in HBE cells.Cell & bioscience · 2020Article
- Ubiquitin ligase TRIM71 suppresses ovarian tumorigenesis by degrading mutant p53.Cell death & disease · 2019Article
- Ionizing radiation induces transgenerational effects of DNA methylation in zebrafish.Scientific reports · 2018Article
- Anatomy of Mdm2 and Mdm4 in evolution.Journal of molecular cell biology · 2017Review
- Dose-dependent effects of gamma radiation on the early zebrafish development and gene expression.PloS one · 2017Article
- Zebrafish as an In Vivo Model to Assess Epigenetic Effects of Ionizing Radiation.International journal of molecular sciences · 2016Review
- Phosphorylation of Def Regulates Nucleolar p53 Turnover and Cell Cycle Progression through Def Recruitment of Calpain3.PLoS biology · 2016Article
- Silver nanoparticles defeat p53-positive and p53-negative osteosarcoma cells by triggering mitochondrial stress and apoptosis.Scientific reports · 2016Article
- Genetic and functional analysis of a Li Fraumeni syndrome family in China.Scientific reports · 2016Article
- Alterations in Mitochondrial and Endoplasmic Reticulum Signaling by p53 Mutants.Frontiers in oncology · 2016Review
- Tumor-specific signaling to p53 is mimicked by Mdm2 inactivation in zebrafish: insights from mdm2 and mdm4 mutant zebrafish.Oncogene · 2015Article
- Mutant p53 accumulates in cycling and proliferating cells in the normal tissues of p53 R172H mutant mice.Oncotarget · 2015Article
- Mutant p53-R273H mediates cancer cell survival and anoikis resistance through AKT-dependent suppression of BCL2-modifying factor (BMF).Cell death & disease · 2015Article
- Aberrant autolysosomal regulation is linked to the induction of embryonic senescence: differential roles of Beclin 1 and p53 in vertebrate Spns1 deficiency.PLoS genetics · 2014Article
- Unequal prognostic potentials of p53 gain-of-function mutations in human cancers associate with drug-metabolizing activity.Cell death & disease · 2014Article
- Heterogeneity of Li-Fraumeni syndrome links to unequal gain-of-function effects of p53 mutations.Scientific reports · 2014Article
- Ribosomal protein mutations induce autophagy through S6 kinase inhibition of the insulin pathway.PLoS genetics · 2014Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutant p53 proteins accumulate to high levels in human tumors and in preneoplastic lesions in the skin and fallopian tube. However examination of tissues from mice and fish that are homozygous for mutant p53 surprisingly showed that the protein was present only at low levels except in the tumors that arose in these animals. The mutant protein did accumulate, however, following treatment with ionizing radiation in the same tissues in which the wild-type protein is induced. Here we study in detail the accumulation of mutant and wild-type p53 proteins following ionizing radiation in zebrafish embryos. We found that the mutant protein was induced by lower levels of radiation and reached higher levels than the wild-type protein. Morpholino knockdown of the zebrafish homologs of Mdm2 and Mdm4 caused dramatic accumulation of mutant p53 protein. The most remarkable results were observed by examining p53 protein levels over an extended time course. Mutant p53 protein increased and persisted for days after irradiation and this was accompanied by persistent elevation of phosphorylated H2AX (γH2AX), implying that the resolution of DNA damage signaling in these embryos is severely compromised by mutations in p53. Thus mutation in p53 results in an exaggerated and persistent damage response, which could in turn drive the process of cancer development as high levels of mutant p53 can act as an oncoprotein to drive invasion and metastasis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.